Richard Possemato

TL;DR: Results reveal that certain breast cancers are dependent upon increased serine pathway flux caused by PHGDH overexpression and demonstrate the utility of in vivo negative-selection RNAi screens for finding potential anticancer targets.

TL;DR: The results demonstrate that loss of Dnmt1 causes cell-type–specific changes in gene expression that impinge on several pathways, including expression of imprinted genes, cell-cycle control, growth factor/receptor signal transduction and mobilization of retroelements.

TL;DR: In this article, a continuous-flow culture apparatus is used to maintain proliferating cancer cells in low-glucose conditions, demonstrating that mitochondrial oxidative phosphorylation (OXPHOS) is essential for optimal proliferation in these conditions; the most sensitive cell lines are defective in OXPHOS upregulation and may therefore be sensitive to current antidiabetic drugs that inhibit OPHOS.

TL;DR: A continuous-flow culture apparatus for maintaining proliferating cells in low-nutrient media for long periods of time is developed and used to undertake competitive proliferation assays, concluding that mtDNA mutations and impaired glucose utilization are potential biomarkers for identifying tumours with increased sensitivity to OXPHOS inhibitors.

TL;DR: It is shown that environmental oxygen levels are a major driver of differential essentiality between in vitro model systems and in vivo tumours, and suppression of NFS1 cooperates with inhibition of cysteine transport to trigger ferroptosis in vitro and slow tumour growth.